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The Journal of Neuroscience, March 16, 2005, 25(11):2885-2894; doi:10.1523/JNEUROSCI.2748-04.2005

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Neurobiology of Disease
Recovery of Myelin after Induction of Oligodendrocyte Cell Death in Postnatal Brain

Walid Jalabi,¹ Nelly Boehm,² Daniel Grucker,¹ and M. Said Ghandour¹

¹Institut de Physique Biologique, Unité Mixte de Recherche 7004, Université Louis Pasteur/Centre National de la Recherche Scientifique, and ²Institut d'Histologie, FacultédeMédecine, 67085 Strasbourg, France

A transgenic mouse line (Oligo-TTK) was established to monitor oligodendrocyte cell death and myelin formation in the CNS. The expression of a conditionally toxic gene, the herpes simplex virus-1 thymidine kinase (HSV1-TK), was made under control of the MBP (myelin basic protein) gene promoter. A truncated form of the HSV1-TK (TTK) gene was used to avoid both bystander effect resulting from leaking in thymidine kinase activity and sterility in transgenic males observed in previous transgenic mice. The transgene was expressed in the CNS with a restricted localization in oligodendrocytes. Oligodendrocyte proliferation and myelin formation are therefore tightly controlled experimentally by administration of ganciclovir (GCV) via the induction of oligodendrocyte cell death. The most severe and irreversible hypomyelination was obtained when GCV was given daily from postnatal day 1 (P1) to P30. Oligodendrocyte plasticity and myelin recovery were analyzed in another phenotype generated by GCV treatment from P1 to P15. In this model, after dysmyelination, an apparent normal behavior was restored with no visible pathological symptoms by P30. Proliferating cells, which may be implicated in myelin repair in this model, are detected primarily in myelin tracts expressing the oligodendrocyte phenotype. Therefore, the endogenous potential of oligodendrocytes to remyelinate was clearly demonstrated in the mice of this study.

Key words: oligodendrocytes; cell death; toxic gene; dysmyelination; myelin recovery; axonal abnormality

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Received July 9, 2004; revised January 26, 2005; accepted February 2, 2005.

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